4 It should be noted that anti-mitochondrial antibody-negative PBC and false-positive anti-transglutaminase antibodies have been reported in this context.19 and 20 As in the case of AIH, the impact of gluten avoidance is not well established, but it is determinant to improve symptomatic CD and to prevent complications.2 and 20 A relation between CD and PSC has been suggested in several case reports and in a population-based study. However the

strength of this association Enzalutamide is not clearly determined and the benefit of gluten exclusion from the diet was not yet demonstrated.2 and 13 Nonalcoholic fatty liver disease (NAFLD) and steatohepatitis (NASH) are common disorders in the general population and in celiac patients. Metformin in vivo Studies found a prevalence of CD in about 3% of individuals with

NAFL and NASH.21 Obesity, a major risk factor for nonalcoholic liver disease, is common in patients with CD not only after but also before gluten withdrawal, which could explain the association between these disorders.22 Additional etiopathogenic mechanisms may be the increased intestinal permeability, resulting in bacterial translocation and production of proinflammatory factors, and malabsorption leading to chronic deficiency of lipotropic molecules.23 and 24 The correlations among CD, obesity and liver disease must be taken into account when establishing the diagnosis and treating celiac patients presenting with elevated liver enzymes. Acute liver failure and advanced liver disease deserve a special consideration. There are several cases reported in literature and CD was found to be Rutecarpine up to 10 times more frequent among patients with chronic liver disease than in the general population.25 The study by Kaukinen and colleagues12 found a high prevalence of CD (4.3%) in patients who underwent liver transplantation. Autoimmune disorders, such as PBC, PSC and AIH were the main etiologies of end-stage liver disease leading to transplantation. This study also describes 4 cases of patients with advanced liver disease

who were found to have CD, all of them improving significantly their liver function with gluten withdrawal. Some of the patients in both groups had no apparent symptoms or signs suggesting CD. The authors emphasize that the early detection and treatment of CD may prevent the progression to end-stage liver failure. Therefore, CD must be screened in patients with autoimmune liver disease or hepatitis/cirrhosis of unknown etiology and in those undergoing liver transplantation. Moreover, an essential component of the clinical surveillance after transplantation in CD patients is the assessment of compliance with a gluten-free diet. The present case illustrates the association between CD and liver disease. Our patient was a young woman presenting with asymptomatic hypertransaminasemia. The initial CD screening was based on autoantibodies, followed by duodenal biopsy.